CAJ | 학술논문

目的观察心肺复苏(CPR)患者外周静脉血中肌酸激酶同工酶(CK-MB)、肌钙蛋白I(cTnI)及心电图ST段抬高的动态变化及冠状动脉(冠脉)造影结果 ,探讨患者CPR后心肌损伤及心肌梗死的诊断及鉴别方法 .方法选择26例CPR且自主循环恢复(ROSC)>24 h的患者,于入院后CPR 0(即刻)、4、8、12、16、20 h抽取外周静脉血检测CK-MB、cTnI活性,ROSC后每隔2 h复查心电图,CK-MB、cTnI活性升高并出现心电图ST段抬高,可疑ST段抬高型心肌梗死(STEMI)者,即进行冠脉造影及介入治疗;无ST段抬高者(C组,5例)不进行冠脉造影检查.冠脉造影显示冠脉血流通畅、未发现梗塞者列为A组(15例);若冠脉主干或分支发现梗塞.出现心肌梗死.即列为B组(6例);D组为15例健康体检者.对各组患者CK-MB、cTnI的动态变化及心电图ST段抬高的程度进行统计学分析.结果 A组CK-MB、cTni于CPR 4 h开始升高,CK-MB于12 h达峰值,cTnI于16 h达峰值,之后逐渐下降;ROSC即刻心电图出现多导联ST段抬高,之后迅速下降,于ROSC 2 h ST段降幅多超过50%.B组CK-MB、cTnl于CPR 4 h开始升高,20 h内逐渐升高;心电图于ROSC即刻出现多导联ST段抬高,2 h后升高的ST段进一步上移.C组CK-MB、cTnI于CPR后逐渐升高,分别于CPR后12 h、16 h达峰值;心电图ST段压低或无明显偏移.D组CK-MB、cTnI在正常范围内表达,心电图ST段无明显偏移.结论 CPR过程中,患者出现了不同程度的心肌损伤,部分患者出现了急性STEMI.CK-MB、cTnI在CPR后逐渐升高,但对心肌损伤与STEMI的早期鉴别无特异性价值.相对而言,心电图具有较早的预测价值:抬高的ST段于ROSC 2 h回降>50%以上,或CK-MB、cTnI酶峰分别前移至CPR 12 h或16 h内多提示心肌损伤;而ROSC 2 h后ST段无回降趋势或CPR 20 h内CK-MB、cTnI逐渐升高多提示合并STEMI,此时需行紧急溶栓或介入治疗.
목적 관찰심폐복소(CPR)환자외주정맥혈중기산격매동공매(CK-MB)、기개단백I(cTnI)급심전도ST단태고적동태변화급관상동맥(관맥)조영결과 ,탐토환자CPR후심기손상급심기경사적진단급감별방법 .방법 선택26례CPR차자주순배회복(ROSC)>24 h적환자,우입원후CPR 0(즉각)、4、8、12、16、20 h추취외주정맥혈검측CK-MB、cTnI활성,ROSC후매격2 h복사심전도,CK-MB、cTnI활성승고병출현심전도ST단태고,가의ST단태고형심기경사(STEMI)자,즉진행관맥조영급개입치료;무ST단태고자(C조,5례)불진행관맥조영검사.관맥조영현시관맥혈류통창、미발현경새자렬위A조(15례);약관맥주간혹분지발현경새.출현심기경사.즉렬위B조(6례);D조위15례건강체검자.대각조환자CK-MB、cTnI적동태변화급심전도ST단태고적정도진행통계학분석.결과 A조CK-MB、cTni우CPR 4 h개시승고,CK-MB우12 h체봉치,cTnI우16 h체봉치,지후축점하강;ROSC즉각심전도출현다도련ST단태고,지후신속하강,우ROSC 2 h ST단강폭다초과50%.B조CK-MB、cTnl우CPR 4 h개시승고,20 h내축점승고;심전도우ROSC즉각출현다도련ST단태고,2 h후승고적ST단진일보상이.C조CK-MB、cTnI우CPR후축점승고,분별우CPR후12 h、16 h체봉치;심전도ST단압저혹무명현편이.D조CK-MB、cTnI재정상범위내표체,심전도ST단무명현편이.결론 CPR과정중,환자출현료불동정도적심기손상,부분환자출현료급성STEMI.CK-MB、cTnI재CPR후축점승고,단대심기손상여STEMI적조기감별무특이성개치.상대이언,심전도구유교조적예측개치:태고적ST단우ROSC 2 h회강>50%이상,혹CK-MB、cTnI매봉분별전이지CPR 12 h혹16 h내다제시심기손상;이ROSC 2 h후ST단무회강추세혹CPR 20 h내CK-MB、cTnI축점승고다제시합병STEMI,차시수행긴급용전혹개입치료.
Objective To observe the change in contents of creatine kinase isoenzyme MB (CK-MB) and cardiac troponin I (cTnI) in peripheral blood, the elevation of ST in electrocardiogram, and the result of coronary arteriongraphy, to identify myocardial damage and acute myocardial infarction during cardiopulmonary resuscitation (CPR). Methods Twenty-six patients with sudden cardiac arrest received CPR, and those patients who had blood circulation maintained for over 24 hours were included. The expression of CK-MB and eTnI activation in peripheral blood were determined at 0, 4, 8, 12, 16 and 20 hours after CPR in all patients. Electrocardiogram was checked every 2 hours in all patients. If CK-MB ,eTnI and ST segment of electrocardiogram was higher than usual, or myocardial infarct with suspicious elevation of ST (STEMI), coronary arteriongraphy and interventional therapy were carried out immediately. Patients were divided into three groups. The patients who were not found to have coronary artery block were classified as group A (15 cases), those who were found to have coronary artery block were group B (6 cases), and the remaining patients in whom ST segment of electrocardiogram did not elevate, and coronary arteriongraphy and interventional therapy were not consider were classified as group C (5 cases). Control group consisted of 15 healthy people (group D). The change in CK-MB and cTnI in peripheral blood and the elevation of electrocardiogram ST segment were analyzed. Results In group A, CK-MB level began to elevate at CPR 4 hours, and it peaked at CPR 12 hours, cTnI began to raise at CPR 4 hours, peaking at CPR 16 hours, then decreased gradually. Elevation of ST was seen in more than two leads in electrocardiogram at the beginning of restoration of spontaneous circulation (ROSC), then lowered quickly, and the decrease exceeded 50% of the elevation at ROSC 2 hours. In group B, the levels of CK-MB and cTnI began to increase at CPR 4 hours, and remained elevated at CPR 20 hours. ST segment was elevated in more than two leads in electrocardiogram at the beginning of ROSC, and remained elevated after ROSC 2 hours. In group C, the CK-MB and cTnI concentrations were increased 4 hours after successful CPR, and reached peak at CPR 12, 16 hours respectively, then they decreased. ST segment of electrocardiogram was not elevated. In group D, the CK-MB and eTnI concentration was in the normal range. ST segment o[electrocardiogram was not elevated. Conclusion All patients manifested myocardial damage after CPR. Some patients showed STEMI after CPR. CK-MB and cTnI concentrations increased gradually after successful CPR without specificity for earlier identification of myocardial damage and STEMI. It is necessary to find a new reliablemarker to check for myocardial damage. Relatively speaking, elevation of the ST segment in electrocardiogram has more predictive value. A decrease exceeds 50% of the elevation of ST segment in electrocardiogram at ROSC 2 hours, or the peak of contents of CK-MB and cTnI appear at CPR 12 hours or 16 hours indicates myocardial damage. If the elevation of ST segment does not descend after ROSC 2 hours, or the levels of CK-MB and cTnl remain elevated at CPR 20 hours, STEMI should be suspected, and it is necessary to undertake interventional therapy or thrombolysis therapy.